ArticleJournal of lipid research2011
An ABCA1-independent pathway for recycling a poorly lipidated 8.1 nm apolipoprotein E particle from glia.
Article in Journal of lipid research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 22 citations in OpenAlex.
- ApoE lipoproteins in the central nervous system under homeostasis and role in Alzheimer's disease and related disorders.Molecular neurodegeneration · 2026Review
- Mechanisms of high-density lipoprotein in regulating blood-brain barrier function: insights and implications.Fluids and barriers of the CNS · 2025Review
- Regulation of glial ApoE secretion by the mevalonate pathway is independent of ApoE isoform.Journal of Alzheimer's disease : JAD · 2025Article
- The cell biology of APOE in the brain.Trends in cell biology · 2024Review
- Axl receptor tyrosine kinase is a regulator of apolipoprotein E.Molecular brain · 2020Article
- Review
- The Important Interface Between Apolipoprotein E and Neuroinflammation in Alzheimer's Disease.Frontiers in immunology · 2020Review
- High-density lipoprotein mimetic peptide 4F mitigates amyloid-β-induced inhibition of apolipoprotein E secretion and lipidation in primary astrocytes and microglia.Journal of neurochemistry · 2018Article
- Small molecule inducers of ABCA1 and apoE that act through indirect activation of the LXR pathway.Journal of lipid research · 2018Article
- Cell-specific production, secretion, and function of apolipoprotein E.Journal of molecular medicine (Berlin, Germany) · 2018Review
- Identification of a Chrysanthemic Ester as an Apolipoprotein E Inducer in Astrocytes.PloS one · 2016Article
- Apolipoprotein E isoform-specific effects on lipoprotein receptor processing.Neuromolecular medicine · 2014Article
- LCAT deficiency does not impair amyloid metabolism in APP/PS1 mice.Journal of lipid research · 2014Article
- Improvement of memory deficits and amyloid-β clearance in aged APP23 mice treated with a combination of anti-amyloid-β antibody and LXR agonist.Journal of Alzheimer's disease : JAD · 2014Article
- Hormonal modulators of glial ABCA1 and apoE levels.Journal of lipid research · 2013Article
- Impact of apolipoprotein E on Alzheimer's disease.Current Alzheimer research · 2013Review
- In vivo measurement of apolipoprotein E from the brain interstitial fluid using microdialysis.Molecular neurodegeneration · 2013Article
- AP-2β regulates amyloid beta-protein stimulation of apolipoprotein E transcription in astrocytes.Brain research · 2012Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Lipid transport in the brain is coordinated by glial-derived lipoproteins that contain apolipoprotein E (apoE) as their primary protein. Here we show that apoE is secreted from wild-type (WT) primary murine mixed glia as nascent lipoprotein subspecies ranging from 7.5 to 17 nm in diameter. Negative-staining electron microscropy (EM) revealed rouleaux, suggesting a discoidal structure. Potassium bromide (KBr) density gradient ultracentrifugation showed that all subspecies, except an 8.1 nm particle, were lipidated. Glia lacking the cholesterol transporter ABCA1 secreted only 8.1 nm particles, which were poorly lipidated and nondiscoidal but could accept lipids to form the full repertoire of WT apoE particles. Receptor-associated-protein (RAP)-mediated inhibition of apoE receptor function blocked appearance of the 8.1 nm species, suggesting that this particle may arise through apoE recycling. Selective deletion of the LDL receptor (LDLR) reduced the level of 8.1 nm particle production by approximately 90%, suggesting that apoE is preferentially recycled through the LDLR. Finally, apoA-I stimulated secretion of 8.1 nm particles in a dose-dependent manner. These results suggest that nascent glial apoE lipoproteins are secreted through multiple pathways and that a greater understanding of these mechanisms may be relevant to several neurological disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.